Boldine Prevents Renal Alterations in Diabetic Rats
Diabetic nephropathy alters both structure and function of the kidney. These alterations are associated with increased levels of reactive oxygen species, matrix proteins, and proinflammatory molecules. Inflammation decreases gap junctional communication and increases hemichannel activity leading to...
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| Format: | Article |
| Language: | English |
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Wiley
2013-01-01
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| Series: | Journal of Diabetes Research |
| Online Access: | http://dx.doi.org/10.1155/2013/593672 |
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| author | Romina Hernández-Salinas Alejandra Z. Vielma Marlene N. Arismendi Mauricio P. Boric Juan C. Sáez Victoria Velarde |
| author_facet | Romina Hernández-Salinas Alejandra Z. Vielma Marlene N. Arismendi Mauricio P. Boric Juan C. Sáez Victoria Velarde |
| author_sort | Romina Hernández-Salinas |
| collection | DOAJ |
| description | Diabetic nephropathy alters both structure and function of the kidney. These alterations are associated with increased levels of reactive oxygen species, matrix proteins, and proinflammatory molecules. Inflammation decreases gap junctional communication and increases hemichannel activity leading to increased membrane permeability and altering tissue homeostasis. Since current treatments for diabetic nephropathy do not prevent renal damage, we postulated an alternative treatment with boldine, an alkaloid obtained from boldo with antioxidant, anti-inflammatory, and hypoglycemic effects. Streptozotocin-induced diabetic and control rats were treated or not treated with boldine (50 mg/Kg/day) for ten weeks. In addition, mesangial cells were cultured under control conditions or in high glucose concentration plus proinflammatory cytokines, with or without boldine (100 µmol/L). Boldine treatment in diabetic animals prevented the increase in glycemia, blood pressure, renal thiobarbituric acid reactive substances and the urinary protein/creatinine ratio. Boldine also reduced alterations in matrix proteins and markers of renal damage. In mesangial cells, boldine prevented the increase in oxidative stress, the decrease in gap junctional communication, and the increase in cell permeability due to connexin hemichannel activity induced by high glucose and proinflammatory cytokines but did not block gap junction channels. Thus boldine prevented both renal and cellular alterations and could be useful for preventing tissue damage in diabetic subjects. |
| format | Article |
| id | doaj-art-aec4614f02f842e991b20a17a1b3dfa7 |
| institution | Kabale University |
| issn | 2314-6745 2314-6753 |
| language | English |
| publishDate | 2013-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Journal of Diabetes Research |
| spelling | doaj-art-aec4614f02f842e991b20a17a1b3dfa72025-08-20T03:39:00ZengWileyJournal of Diabetes Research2314-67452314-67532013-01-01201310.1155/2013/593672593672Boldine Prevents Renal Alterations in Diabetic RatsRomina Hernández-Salinas0Alejandra Z. Vielma1Marlene N. Arismendi2Mauricio P. Boric3Juan C. Sáez4Victoria Velarde5Departamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDepartamento de Fisiología, Pontificia Universidad Católica de Chile, Alameda Bernardo O’Higgins, No. 340, 6513677 Santiago, ChileDiabetic nephropathy alters both structure and function of the kidney. These alterations are associated with increased levels of reactive oxygen species, matrix proteins, and proinflammatory molecules. Inflammation decreases gap junctional communication and increases hemichannel activity leading to increased membrane permeability and altering tissue homeostasis. Since current treatments for diabetic nephropathy do not prevent renal damage, we postulated an alternative treatment with boldine, an alkaloid obtained from boldo with antioxidant, anti-inflammatory, and hypoglycemic effects. Streptozotocin-induced diabetic and control rats were treated or not treated with boldine (50 mg/Kg/day) for ten weeks. In addition, mesangial cells were cultured under control conditions or in high glucose concentration plus proinflammatory cytokines, with or without boldine (100 µmol/L). Boldine treatment in diabetic animals prevented the increase in glycemia, blood pressure, renal thiobarbituric acid reactive substances and the urinary protein/creatinine ratio. Boldine also reduced alterations in matrix proteins and markers of renal damage. In mesangial cells, boldine prevented the increase in oxidative stress, the decrease in gap junctional communication, and the increase in cell permeability due to connexin hemichannel activity induced by high glucose and proinflammatory cytokines but did not block gap junction channels. Thus boldine prevented both renal and cellular alterations and could be useful for preventing tissue damage in diabetic subjects.http://dx.doi.org/10.1155/2013/593672 |
| spellingShingle | Romina Hernández-Salinas Alejandra Z. Vielma Marlene N. Arismendi Mauricio P. Boric Juan C. Sáez Victoria Velarde Boldine Prevents Renal Alterations in Diabetic Rats Journal of Diabetes Research |
| title | Boldine Prevents Renal Alterations in Diabetic Rats |
| title_full | Boldine Prevents Renal Alterations in Diabetic Rats |
| title_fullStr | Boldine Prevents Renal Alterations in Diabetic Rats |
| title_full_unstemmed | Boldine Prevents Renal Alterations in Diabetic Rats |
| title_short | Boldine Prevents Renal Alterations in Diabetic Rats |
| title_sort | boldine prevents renal alterations in diabetic rats |
| url | http://dx.doi.org/10.1155/2013/593672 |
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